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Innovations in Early Cancer Diagnostics and Therapeutics

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 8814

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Special Issue Editors

Dr. Seddik Hammad

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Guest Editor

Molecular Hepatology Section, Department of Medicine II, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
Interests: chronic liver diseases; liver cancer; systems medicine; computational modelling; bioinformatics; OMICS

Dr. Mohamed Bekheit

E-Mail Website
Guest Editor

Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK
Interests: liver cancer; early diagnosis; screening; cancer cure; surgical sciences; interventional procedures

Special Issue Information

Dear Colleagues,

Cancer is a leading cause of death worldwide, accounting for nearly 10 million deaths in 2020, representing nearly one in six deaths. Many cancers can be cured if detected/diagnosed early and treated effectively; however, they are mostly diagnosed at advanced stages when systemic therapies are indicated. Therefore, preclinical studies are required and should be coupled with clinical investigations to identify a robust and reliable method for identifying/diagnosing patients in the very early stages of cancer development. Not only prognostic/diagnostic values, but also the targets can be used to combat the disease development, progression and metastasis. Authors are invited to submit manuscripts that delineate these cancer-assigned prognostic, diagnostic and therapeutical targets (pathways). Data may provide useful information and clinical rationale concerning how to better and more accurately diagnose human cancers with the goal to foster therapeutic interventions. In this Special Issue, original research articles and reviews are welcome to shed light on the state-of-the-art, as well as novel data, contributing to identifying prognostic and diagnostic targets in the development and progression of human cancer.

We welcome experts in the field to contribute research papers and critical reviews regarding the various facets of preclinical to clinical investigations that modulate cancer development and progression, as well as on how natural and pharmacological pathways may be exploited as tools in anticancer therapies.

Dr. Seddik Hammad
Dr. Mohamed Bekheit
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

solid cancer
cancers
chemotherapy
cancer inhibitors
cancer pathways
prognostic markers
preclinical cancers

Published Papers (4 papers)

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Research

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18 pages, 3583 KiB

Open AccessArticle

Changes in Nucleolin Expression during Malignant Transformation Leading to Ovarian High-Grade Serous Carcinoma

by Elizabeth A. Paris, Janice M. Bahr, Sanjib Basu and Animesh Barua

Cancers 2023, 15(3), 661; https://doi.org/10.3390/cancers15030661 - 21 Jan 2023

Cited by 1 | Viewed by 1768

Abstract

Objective: Ovarian high-grade serous carcinoma (HGSC) is a fatal malignancy of women. Alterations in the expression of nuclear proteins are early steps in malignant transformation; nucleolin is one such protein. Changes in nucleolin expression and circulatory levels during ovarian HGSC development are unknown. The study goal was to determine if tissue and circulatory levels of nucleolin change in response to malignant transformation leading to ovarian HGSC. Methods: Sera, ovaries, and BRCA+ fimbria from healthy subjects, and sera and tumor tissues from patients (n = 10 each), and healthy hens and hens with HGSC were examined in exploratory and prospective studies for nucleolin expression by immunohistochemistry, immunoblotting, gene expression, and immunoassay, and analyzed by analysis of variance (ANOVA). Results: Compared with normal, nucleolin expression was higher in patients and hens with ovarian HGSC and in women with a risk of HGSC (P < 0.05). Compared with normal (1400 + 105 pg/mL, n = 8), serum nucleolin levels were 1.5 and 1.7-fold higher in patients with early- (n = 5) and late-stage (n = 5) HGSC, respectively. Additionally, serum nucleolin levels increased significantly (P < 0.05) prior to the formation of detectable masses. Conclusion: This pilot study concluded that tissue and serum levels of nucleolin increase in association with malignant changes in ovaries and fimbriae leading to ovarian HGSC. Full article

(This article belongs to the Special Issue Innovations in Early Cancer Diagnostics and Therapeutics)

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23 pages, 3724 KiB

Open AccessArticle

c-MYC Protein Stability Is Sustained by MAPKs in Colorectal Cancer

by Martina Lepore Signorile, Valentina Grossi, Candida Fasano, Giovanna Forte, Vittoria Disciglio, Paola Sanese, Katia De Marco, Francesca La Rocca, Raffaele Armentano, Anna Maria Valentini, Gianluigi Giannelli and Cristiano Simone

Cancers 2022, 14(19), 4840; https://doi.org/10.3390/cancers14194840 - 4 Oct 2022

Cited by 5 | Viewed by 2123

Abstract

c-MYC is one of the most important factors involved in colorectal cancer (CRC) initiation and progression; indeed, it is found to be upregulated in up to 80% of sporadic cases. During colorectal carcinogenesis, c-MYC is maintained upregulated through β-catenin-mediated transcriptional activation and ERK-mediated post-translational stabilization. Our data demonstrate that p38α, a kinase involved in CRC metabolism and survival, contributes to c-Myc protein stability. Moreover, we show that p38α, like ERK, stabilizes c-MYC protein levels by preventing its ubiquitination. Of note, we found that p38α phosphorylates c-MYC and interacts with it both in vitro and in cellulo. Extensive molecular analyses in the cellular and in vivo models revealed that the p38α kinase inhibitors, SB202190 and ralimetinib, affect c-MYC protein levels. Ralimetinib also exhibited a synthetic lethality effect when used in combination with the MEK1 inhibitor trametinib. Overall, our findings identify p38α as a promising therapeutic target, acting directly on c-MYC, with potential implications for countering c-MYC-mediated CRC proliferation, metastatic dissemination, and chemoresistance. Full article

(This article belongs to the Special Issue Innovations in Early Cancer Diagnostics and Therapeutics)

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23 pages, 2503 KiB

Open AccessArticle

Critical Investigation of the Usability of Hepatoma Cell Lines HepG2 and Huh7 as Models for the Metabolic Representation of Resectable Hepatocellular Carcinoma

by Gerda Schicht, Lena Seidemann, Rene Haensel, Daniel Seehofer and Georg Damm

Cancers 2022, 14(17), 4227; https://doi.org/10.3390/cancers14174227 - 30 Aug 2022

Cited by 5 | Viewed by 2260

Abstract

Metabolic alterations in hepatocellular carcinoma (HCC) are fundamental for the development of diagnostic screening and therapeutic intervention since energy metabolism plays a central role in differentiated hepatocytes. In HCC research, hepatoma cell lines (HCLs) like HepG2 and Huh7 cells are still the gold standard. In this study, we characterized the metabolic profiles of primary human hepatoma cells (PHCs), HCLs and primary human hepatocytes (PHHs) to determine their differentiation states. PHCs and PHHs (HCC-PHHs) were isolated from surgical specimens of HCC patients and their energy metabolism was compared to PHHs from non-HCC patients and the HepG2 and Huh7 cells at different levels (transcript, protein, function). Our analyses showed successful isolation of PHCs with a purity of 50–73% (CK18+). The transcript data revealed that changes in mRNA expression levels had already occurred in HCC-PHHs. While many genes were overexpressed in PHCs and HCC-PHHs, the changes were mostly not translated to the protein level. Downregulated metabolic key players of PHCs revealed a correlation with malign transformation and were predominantly pronounced in multilocular HCC. Therefore, HCLs failed to reflect these expression patterns of PHCs at the transcript and protein levels. The metabolic characteristics of PHCs are closer to those of HCC-PHHs than to HCLs. This should be taken into account for future optimized tumor metabolism research. Full article

(This article belongs to the Special Issue Innovations in Early Cancer Diagnostics and Therapeutics)

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Review

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24 pages, 2180 KiB

Open AccessReview

Insight into the Crosstalk between Photodynamic Therapy and Immunotherapy in Breast Cancer

by Hongzhong Jin, Shichong Liao, Feng Yao, Juanjuan Li, Zhiliang Xu, Kailiang Zhao, Ximing Xu and Shengrong Sun

Cancers 2023, 15(5), 1532; https://doi.org/10.3390/cancers15051532 - 28 Feb 2023

Cited by 10 | Viewed by 2032

Abstract

Breast cancer (BC) is the world’s second most frequent malignancy and the leading cause of mortality among women. All in situ or invasive breast cancer derives from terminal tubulobular units; when the tumor is present only in the ducts or lobules in situ, it is called ductal carcinoma in situ (DCIS)/lobular carcinoma in situ (LCIS). The biggest risk factors are age, mutations in breast cancer genes 1 or 2 (BRCA1 or BRCA2), and dense breast tissue. Current treatments are associated with various side effects, recurrence, and poor quality of life. The critical role of the immune system in breast cancer progression/regression should always be considered. Several immunotherapy techniques for BC have been studied, including tumor-targeted antibodies (bispecific antibodies), adoptive T cell therapy, vaccinations, and immune checkpoint inhibition with anti-PD-1 antibodies. In the last decade, significant breakthroughs have been made in breast cancer immunotherapy. This advancement was principally prompted by cancer cells’ escape of immune regulation and the tumor’s subsequent resistance to traditional therapy. Photodynamic therapy (PDT) has shown potential as a cancer treatment. It is less intrusive, more focused, and less damaging to normal cells and tissues. It entails the employment of a photosensitizer (PS) and a specific wavelength of light to create reactive oxygen species. Recently, an increasing number of studies have shown that PDT combined with immunotherapy improves the effect of tumor drugs and reduces tumor immune escape, improving the prognosis of breast cancer patients. Therefore, we objectively evaluate strategies for their limitations and benefits, which are critical to improving outcomes for breast cancer patients. In conclusion, we offer many avenues for further study on tailored immunotherapy, such as oxygen-enhanced PDT and nanoparticles. Full article

(This article belongs to the Special Issue Innovations in Early Cancer Diagnostics and Therapeutics)

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